ArticleCancer research2014
Cyclophilin B supports Myc and mutant p53-dependent survival of glioblastoma multiforme cells.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Links between the unfolded protein response and the DNA damage response in hypoxia: a systematic review.Biochemical Society transactions · 2021Pooled it
- Identification of glycometabolism-related genes for predicting the prognosis of patients with glioblastoma and its correlation with immune infiltration.Discover oncology · 2026Article
- A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury.Cell reports. Medicine · 2026Article
- Prognostic Significance and Functional Role of PPIB in a Retrospective Cohort of Patients with Advanced Gastric Cancer.Oncology research · 2026Article
- Article
- A Novel Chemotherapy Combination to Enhance Proteotoxic Cell Death in Hepatocellular Carcinoma Experimental Models Without Killing Non-Cancer Cells.International journal of molecular sciences · 2025Article
- Dose-Dependent Transcriptional Response to Ionizing Radiation Is Orchestrated with DNA Repair within the Nuclear Space.International journal of molecular sciences · 2024Article
- Cyclophilin inhibition as a strategy for the treatment of human disease.Frontiers in pharmacology · 2024Review
- PPIB/Cyclophilin B expression associates with tumor progression and unfavorable survival in patients with pulmonary adenocarcinoma.American journal of cancer research · 2024Article
- Article
- High-fat diet induced cyclophilin B enhances STAT3/lncRNA-PVT1 feedforward loop and promotes growth and metastasis in colorectal cancer.Cell death & disease · 2022Article
- Article
- Lysyl hydroxylase 2 mediated collagen post-translational modifications and functional outcomes.Scientific reports · 2022Article
- Article
- The Role of Cyclophilins in Inflammatory Bowel Disease and Colorectal Cancer.International journal of biological sciences · 2021Review
- Cyclophilin B overexpression predicts a poor prognosis and activates metastatic pathways in colon cancer.Translational cancer research · 2020Article
- A Pan-Cyclophilin Inhibitor, CRV431, Decreases Fibrosis and Tumor Development in Chronic Liver Disease Models.The Journal of pharmacology and experimental therapeutics · 2019Article
- The Multiple Roles of Peptidyl Prolyl Isomerases in Brain Cancer.Biomolecules · 2018Review
- Cycloheximide promotes paraptosis induced by inhibition of cyclophilins in glioblastoma multiforme.Cell death & disease · 2017Article
- Protein synthesis inhibition enhances paraptotic death induced by inhibition of cyclophilins in glioblastoma cells.Cancer cell & microenvironment · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Glioblastoma multiforme is an aggressive, treatment-refractory type of brain tumor for which effective therapeutic targets remain important to identify. Here, we report that cyclophilin B (CypB), a prolyl isomerase residing in the endoplasmic reticulum (ER), provides an essential survival signal in glioblastoma multiforme cells. Analysis of gene expression databases revealed that CypB is upregulated in many cases of malignant glioma. We found that suppression of CypB reduced cell proliferation and survival in human glioblastoma multiforme cells in vitro and in vivo. We also found that treatment with small molecule inhibitors of cyclophilins, including the approved drug cyclosporine, greatly reduced the viability of glioblastoma multiforme cells. Mechanistically, depletion or pharmacologic inhibition of CypB caused hyperactivation of the oncogenic RAS-mitogen-activated protein kinase pathway, induction of cellular senescence signals, and death resulting from loss of MYC, mutant p53, Chk1, and Janus-activated kinase/STAT3 signaling. Elevated reactive oxygen species, ER expansion, and abnormal unfolded protein responses in CypB-depleted glioblastoma multiforme cells indicated that CypB alleviates oxidative and ER stresses and coordinates stress adaptation responses. Enhanced cell survival and sustained expression of multiple oncogenic proteins downstream of CypB may thus contribute to the poor outcome of glioblastoma multiforme tumors. Our findings link chaperone-mediated protein folding in the ER to mechanisms underlying oncogenic transformation, and they make CypB an attractive and immediately targetable molecule for glioblastoma multiforme therapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.